Rockefeller Inclusive Science Initiative Guest Lecture

Event Details

The “discoordination” hypothesis asserts that a common pathophysiology underlies the failures of cognitive function that are characteristic of mental inflexibility and failures of cognitive control as observed in a variety of clinical conditions, including autism. The hypothesis derives from the notion that neural computations within and between networks of cells depend upon temporally coordinated neural activity and cognitive impairment emerges when this coordination is sufficiently aberrant. This neural coordination is thought to derive from inappropriate excitatory and inhibitory synaptic transmission that interferes with the ability of neurons to temporally organize their electrical discharge to maintain and switch between separate streams of information flow through neuronal networks. Fenton will describe his lab's approach to understanding cognition and cognitive dysfunction as a systems problem at multiple levels of biological organization. He will focus on work demonstrating that the microstructure of the time series of spatially organized oscillatory events in the local field potential of hippocampus organizes the discharge of principal cells, depends on experience, indicates the subject’s current knowledge, and reveals explains cognitive inflexibility abnormalities in Fmr1-null mutant mice that model the genetic defect that causes Fragile X Syndrome.

Rockefeller's reaccreditation from the Association for the Accreditation of Human Research Protection Programs marks the end of an extensive application process. The AAHRPP sets the gold standard in safeguarding volunteers participating in clinical research.